Kimberly Jasmer, PhD

Assistant Research Professor


Contact Information

Phone 573-882-1708
Address 540F Bond Life Sciences Center


  • BS, Cellular, Molecular, and Developmental Biology, University of Washington, Seattle, WA, 2009
  • PhD, Biological Sciences, University of Missouri, Columbia, MO, 2015

Research Interests

My work focuses on the immunopathogenesis of inflammatory disorders of the salivary glands, namely the autoimmune disease Sjögrens syndrome (SS) and chronic hyposalivation as a collateral side effect of head and neck cancer radiotherapy. I’m especially interested in understanding how Damage Associated Molecular Patterns (DAMPs) coordinate epithelial-immune cell communication in these pathogenic processes.

Research Description

Current Projects

Nucleotide Receptors and Sjögrens Syndrome Pathogenesis

Sjögren’s syndrome (SS) is a chronic, inflammatory autoimmune disease that is characterized by lymphocytic infiltration of the lacrimal and salivary glands, resulting in dry eye and dry mouth, respectively, though it is a systemic disease that also affects other exocrine and non-exocrine tissues. Salivary gland hypofunction in SS results in increased incidence of periodontitis, yeast and bacterial infections, and digestive disorders. SS can present in isolation as primary (pSS) or secondary SS in conjunction with other systemic autoimmune conditions such as rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE). B cells play an important role in the pathogenesis of SS and indicators of B cell hyperactivity in SS include production of autoantibodies, hypergammaglobulinemia and development of B cell lymphomas. 

We have investigated how release from damaged cells of cytoplasmic nucleotides, such as adenosine 5’-triphosphate (ATP), acts as an extracellular DAMP to initiate chronic inflammatory responses through activation of P2 nucleotide receptors, including ATP-gated ionotropic P2X receptors and G protein-coupled P2Y receptors. Recently, we found that the G protein-coupled P2Y2 receptor (P2Y2R) is functionally expressed in salivary gland-infiltrating B cells where P2Y2R activation mediates B cell migration and cytokine release. We have also demonstrated that antagonism or genetic deletion of this receptor resolves lymphocytic infiltration of the salivary gland and restores salivary function in mouse models of SS.

In addition to glandular pathology, pulmonary manifestations have been reported in 10-20% of SS patients. SS patients also can exhibit neurological disorders and hematological conditions, the most severe of which are B cell lymphomas. Our current studies aim to determine whether P2Y2R antagonism in an SS mouse model mitigates the risk of B cell lymphoma development. We found that in the IL-14α transgenic (TG) mouse model of SS, which overexpresses human IL-14α, associated inflammation is not restricted to secretory organs, such as the salivary and lacrimal glands, but is manifested systemically including in the lung, kidney and liver.

While this work is ongoing, our preliminary data suggest a role for P2Y2R in systemic manifestations in two mouse models of SS and that P2Y2R antagonism enhances saliva flow. The long-term goal of this project is to evaluate whether P2Y2R antagonism is a general approach for treatment of chronic inflammatory diseases.

Radiation-Induced Hyposalivation

Following radiotherapy (RT) for the treatment of head and neck cancer (HNC), collateral damage to surrounding tissues, such as salivary glands, is a significant problem. Over 80% of HNC patients will experience RT-induced xerostomia (i.e., dry mouth), the majority of whom will never regain function. Chronic hypofunction results in changes in saliva quality (e.g., pH, composition, viscosity), increased incidence of dental caries and oral infections, periodontitis, difficulties with swallowing and speaking and nutritional deficiencies, all of which can affect the quality of life for patients. Previous studies in patients receiving RT for HNC have suggested that acute dysfunction results from disruption of acinar epithelial cells that secrete saliva, whereas chronic dysfunction may result from additional factors, such as glandular atrophy, lymphocytic infiltration (i.e., sialadenitis) and periductal and parenchymal fibrosis.

The immunomodulatory effect of RT has been described in multiple contexts, including in thoracic RT, which can result in inflammation of the lung (i.e., pneumonitis) and pulmonary fibrosis. Several mechanisms for this response have been proposed, including activation and proliferation of immune cells, such as dendritic cells, and enhanced chemokine and cytokine release. Previous studies have utilized mouse models of targeted head and neck irradiation to investigate mechanisms of salivary dysfunction, stem cell function and regeneration. However, few studies have investigated the immune response in the salivary glands following RT and the contributions of sustained inflammation to chronic dysfunction have not been explored. In contrast, acute events following exposure to ionizing radiation (IR) are well studied. Targeting the inflammatory response after the acute phase and prior to irreparable glandular damage may be a strategy for preventing chronic hypofunction. To identify potential therapeutics and effective timing for administration, we must first have a more detailed understanding of the immunological processes involved.

The epithelium plays a significant role in responding to insults and coordinating an immune response. This interplay between epithelial and immune cells has been reported in models of infection and autoimmune disease of the SG epithelium, i.e., Sjögrens syndrome, and as a result of ionizing radiation. Following irradiation, human and murine cells release ATP that we have demonstrated in murine parotid salivary gland epithelial cells serves to activate the ionotropic P2X7 receptor (P2X7R). The lab of Dr. Gary Weisman has demonstrated that activation of P2X7R results in the release of IL-1β, which upregulates the G protein-coupled P2Y2 receptor (P2Y2R), a well-studied mediator of localized immune responses. We hypothesize that IR-induced ATP release causes P2X7R-dependent upregulation of the P2Y2R in SG epithelial and immune cells, whereupon P2Y2R activation by released ATP mediates immune cell recruitment, proliferation, and activation, thereby contributing to long-term inflammation, fibrosis and salivary hypofunction.

Our preliminary data indicate a robust immune response in both humans and mice at chronic time points following head and neck irradiation. The long-term goals of this project are to 1) generate a timeline of immune responses following irradiation, 2) investigate the role of the P2Y2R in mediating these immune responses, and 3) evaluate whether P2Y2R antagonism is a novel therapeutic modality to prevent chronic radiation-induced salivary gland dysfunction.

Notable Honors and Service

  • International Association for Dental Research (IADR), Salivary Research Award (2021)
  • Search Committee for Director of Postdoctoral Education at the University of Missouri (2021)
  • Group Program Chair for the American and International Associations For Dental Research (AADR/IADR) Salivary Research Group (2020-2023)
  • Invited Talk at the NIH Geroscience Interest Group Postdoctoral Symposium on Tissue-Resident Immune Cells (2019)
  • University of Missouri Postdoctoral Research Grant (2019)
  • University of Missouri Postdoctoral Education Advisory Council (PEAC) (2019-2021)
  • University of Missouri Postdoctoral Association (Chair: 2019-2021; Professional Development Chair: 2018-2019)
  • Sjögren’s Syndrome Foundation Research Grant (2018-2021)
  • Invited Talk at Salivary Glands and Exocrine Biology Gordon Research Conference (2017)
  • Associate Teaching Certification, University of Missouri and Center for the Integration of Research, Teaching, and Learning (CIRTL) (2016)
  • Joshua E. Neimark Memorial Travel Assistance Award from the American Association for the Advancement of Science (AAAS) (2015)
  • GAANN Fellowship from the U.S. Department of Education (2010-2014)

Selected Publications

Kimberly J Jasmer, Lucas T Woods, Kevin Muñoz Forti, Adam L Martin, Jean M Camden, Marco Colonna, and Gary A Weisman. P2Y2 Receptor Antagonism Inhibits Inflammation in a Mouse Model of Sjögren’s Syndrome. Arch. Oral Biol. 2021 Apr;124:105067. doi: 10.1016/j.archoralbio.2021.105067. PMCID: PMC7958986

Kimberly J Jasmer, Kristy E Gilman, Kevin Muñoz Forti, Gary A Weisman, and Kirsten H Limesand. Radiation-Induced Salivary Gland Dysfunction: Mechanisms, Therapeutics, and Future Directions. J. Clin. Med. 2020, 9, 4095. doi: 10.3390/jcm9124095. PMCID: PMC7767137

Vinit C. Shanbhag, Nikita Gudekar, Kimberly Jasmer, Christos Papageorgiou, Kamal Singh, and Michael J. Petris. Copper Metabolism as a Unique Vulnerability in Cancer. Biochim Biophys Acta Molecular Cell Research. 2020. doi: 10.1016/j.bbamcr.2020.118893. PMCID: PMC7572722

Kimberly J Jasmer, J Hou, P Mannino, J Cheng, and Mark Hannink. Role of Heme Oxygenase Promotes B-Raf-dependent Melanosphere Formation. Pigment Cell Melanoma Res. 2020; doi: 10.1111/pcmr.12905. PMCID: PMC7572722

Lucas T Woods, Kimberly J Jasmer, Kevin Muñoz Forti, Vinit C Shanbhag, Jean M Camden, Laurie Erb, Michael J Petris, and Gary A. Weisman. P2Y2 Receptors Mediate Nucleotide-induced EGFR Phosphorylation and Stimulate Proliferation and Tumorigenesis of Human Oral Cancer Cells. Oral Oncol. 2020;109:104808. doi: 10.1016/j.oraloncology.2020.104808. PMCID: PMC7736485

Mahmoud G Khalafalla, Lucas T Woods, Kimberly J Jasmer, Kevin Muñoz Forti, Jean M Camden, Janicke L Jensen, Kirsten H Limesand, Hilde K Galtung, and Gary A Weisman. P2 Receptors as Therapeutic Targets in the Salivary Gland: From Physiology to Dysfunction. Front in Pharmacol. 2020;11:222. doi: 10.3389/fphar.2020.00222. PMCID: PMC7082426.

Vinit C Shanbhag , Kimberly Jasmer-McDonald, Sha Zhu, Adam L Martin, Nikita Gudekar, Aslam A Khan, Erik Ladomersky, Kamalendra Singh, Gary A Weisman , and Michael J Petris. ATP7A Delivers Copper to the Lysyl Oxidase Family of Enzymes and Promotes Tumorigenesis and Metastasis. zProc Natl Acad Sci US A. 2019;116(14):6836-41. doi: 10.1073/pnas.1817473116. PMCID: PMC6452744.

Grace Y Sun, Z Chen, Kimberly J Jasmer, Dennis Y Chuang, Zezong Gu, Mark Hannink, and Agnes Simonyi. Quercetin Attenuates Inflammatory Responses in BV-2 Microglial Cells: Role of MAPKs on the Nrf2 Pathway and Induction of Heme Oxygenase-1. PLoS One. 2015;10(10):e0141509. doi: 10.1371/journal.pone.0141509. PMCID: PMC4624710.

Otis C Attucks, Kimberly J Jasmer,  Mark Hannink, Jareer Kassis, Zhenping Zhong, Suparna Gupta, Sam F Victory, Mustafa Guzel, Dharma Rao Polisetti, Robert Andrews, Adnan MM Mjalli, and Matthew J Kostura. Induction of Heme Oxygenase I (HMOX1) by HPP-4382: A Novel Modulator of Bach1 Activity. PLoS One. 2014;9(7):e101044. doi: 10.1371/journal.pone.0101044. PMCID: PMC4096395

Full list of publications can be found here.